Straightening Out The Arachidonic Acid Debate

Written by: Kevin Cann

After talking to a few of my fellow peers I realized there was still a misunderstanding out there about animal fats, especially arachidonic acid. Most people believe arachidonic acid should be kept to a minimum in the diet because of its pro-inflammatory effects. This means our diets would have to limit liver, egg yolks, and animal fats.

Contrary to popular beliefs, animal fats only contain a small amount of arachidonic acid and grass fed meat tends to have less than conventional meats. When cells are damaged by oxidation, eicosanoids are formed from the arachidonic acid. Examples of eicosanoids are prostaglandins, prostacyclins, thromboxanes, and leukotrienes. These eicosanoids have numerous important roles in our body in our inflammation response, generating fever, and regulation of blood pressure, blood clotting, immune system regulation, reproduction control, tissue growth, and our sleep cycle (Diwan, 2008).

All of those functions in which arachidonic acid plays a role are critical to our health. Without them we would die prematurely and cease to exist as a species. This alone makes limiting arachidonic acid dangerous. In fact, NSAIDs work by down regulating the eicosanoids and that is how they control inflammation, fever, and clotting. A study performed by Chan and colleagues showed the dangers of limiting these eicosanoids via NSAIDs. This study was looking at arthritis and its resolution. Chan stated that prostaglandin e2 was present during resolution and is essential for LIMITING chronic inflammation in autoimmune arthritis (Chan, 2010). This study shows that AA also has an anti-inflammatory role as well.

Being deficient in AA has some negative effects including hair loss, skin issues, and infertility (Masterjohn, 2012). AA deficiency also has a role in mental illness. AA is the most abundant fat found in the brain. Research has linked low levels of AA to schizophrenia, depression, and bipolar disorder. This is attributed to the AA leaking out of the cells. This is theorized to be the reason that MRIs of mentally ill patients show less brain matter (Campbell-McBride, 2010). Natasha Campbell-McBride has an interesting explanation in her Gut and Psychology Syndrome book. She points to research that blames the AA leakage on phospholipase A2 (PLA2). PLA2 is an enzyme whose role is to release AA from the cell. This enzyme becomes overactive in patients presenting with mental illness. She blames the enzyme overactivity on the pathogens allowed to enter the bloodstream from a damaged gut lining. She also states that chronic inflammation activates PLA2 (Campbell-McBride, 2010).

AA is actually responsible for creating cell junctions to protect us from pathogens. If there are pathogens causing AA to decrease in cell membranes then even more pathogens are going to be allowed to do damage to healthy cells. To make matters even worse we may be limiting AA in our diet which furthers our deficiency.

In conclusion, AA got a bad rap somewhere along the way. AA is essential to our health and without it we can have numerous health problems including immune dysregulation, skin issues, infertility, and even mental illness. We need to trust Mother Nature more in terms of what we put into our bodies. We need to trust that the ratios of nutrients in real foods are the ratios that will allow us to thrive as a species. They have been there for millions of years and have gotten us this far. Once we changed them it seemed we started running into health problems.

Kevin is owner of Genetic Potential Nutrition. He is a holistic nutritionist, wellness coach, and strength coach. He works with people fighting illness, to competitive athletes. Check out his site at www.geneticpotentialnutrition.com.

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Christopher Williams (a.k.a. Squatchy) is a paleo aficionado, educator, personal trainer, wellness coach, and hobbyist chef. He also works as part of the Robb Wolf team.

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Comments

Isn’t it mostly the n-6 from industrial lubricants (aka vegetable seed oils) that we put into our bodies that are cause of the bad rap? (which conventional wisdom for whatever reason manages to project onto animal products)

Well, this certainly would help explain why my sister’s indeterminent mood disorder was worse when she lived on her own and ate mostly vegetarian but got better when she moved in with her fiance, who provides most of their meat, through hunting

This is one reason why grassfed meats are recommended, the O3:O6 ratio is more in balance. It is when the O6 PUFAs get way out of control that we will run into problems. AA is just a small part of the fats found in meat also.

Would this apply to those who have suffered multiple concussions and have been screened for mental illness with (questionable) negative findings? Would there be an “increased” need for those with head injuries through sports?

Hi Kevin, I hear what you are saying and agree with you and your references for the most part, but what about the aspect of AA which was noted by the Eades in the Protein Power books, primarily its effect on cholesterol levels. I know we shouldn’t worry so much about cholesterol, and about lipoprotein A versus B and the details of how inflammation of arterial intima occurs, due primarily to excess carb intake and high O6, but as many in the paleo community have observed, some of us tend to see very high increases in total chol and in general LDL levels, which regardless of the lipoprotein fractions A and B and their ratios, tends to suggest an increase in inflammation. These increases tend to be most heavily associated with out of proportion increases in intake of eggs and red meats, without enough variety and other protein sources such as fish, seafood, etc. For example, my chol levels almost doubled when I was eating 12 eggs a day, every day for 3 months, but dropped back to normal when I just started having sardines for breakfast. So I would suggest that we not tell people to start eating heavily of AA laden foods, but rather to include them judiciously, as part of a varied protein intake including other, more anti-imflammatory sources (e.g. grass feed beef, seafood, etc.). I guess I am just trying to say that egg consumption can lead you down the wrong path if not done in moderation. Thoughts?

12 eggs is impressive… I don’t think most people can do that. Kudos. I wish I could find the study but it’s buried in my old college notebooks in a box somewhere, but there are people who can eat tons of eggs and have no change in cholesterol. So some people may be stronger responders than others. I agree that a safe recommendation would be that it’s ok to include higher AA protein sources but as part of a varied diet. Everyone is so different, it’s best to be careful when making nutritional recommendations. Good info.

Maybe arachidonic acid created from excess linoleic acid behaves differently from the ARA in animal fats.
ARA may be low in the brains of schizophrenics in part because there is more lipolysis (fat burning) going on there. The niacin flush is due to PGD2 and PGE2 and schizophrenics are less sensitive to this effect.
“Once niacin is ingested, it acts by binding to a receptor on cells beneath the skin. This receptor is known as the G-protein coupled receptor 109A (GPR109A). It is present on the surface of spindle-shaped cells called Langerhans cells. Once activated, the Langerhans cells begin to release two types of prostaglandin molecules, PGD2 and PGE2.”
Jeff Volek found that ARA is preserved in very low carb dieters – there is more of it, because less is being converted to prostaglandins.
So more ARA does not always mean more inflammation; this is driven by carbs, not lipids.
“It has been postulated that during liver damage there is an arachidonic acid metabolism deflection toward lipoxygenase products and a simultaneous decrement of the synthesis of cytoprotective prostaglandins. Accordingly, we have demonstrated that leukotriene synthesis inhibition protects the liver from acute damage induced by CCI4. Thus, the aim of the present work was to study the effect of caffeic acid (a specific 5-lipoxygenase inhibitor) on liver cirrhosis induced by CCI4 administration in the rat.”

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